Osmotic Demyelination Syndrome due to Rhabdomyolysis and Hyperosmolar Hyperglycemic Syndrome following Cardiogenic Shock.

Osmotic demyelination syndrome (ODS) is a relatively rare disease that causes rapid demyelination, resulting in pontine and central nervous system damage with various symptoms, including impaired consciousness. It often occurs when hyponatremia is rapidly corrected. However, it can also occur when a normonatremic patient suddenly develops hypernatremia. A 51-year-old man developed cardiogenic shock with impaired consciousness, hyperCKemia, hypernatremia, and hyperglycemia. Osmotic demyelination syndrome secondary to rhabdomyolysis and hyperosmolar hyperglycemic syndrome was suspected. The patient's fluid volume decreased because of osmotic diuresis caused by hyperglycemia, and the blood sodium level increased rapidly. The latter resulted in ODS, which in turn resulted in a prolonged disturbance of consciousness, from which he has not yet recovered. ODS has been reported as a serious complication of rapid correction of hyponatremia, although it also occurs when normonatremia leads to hypernatremia. This disease is difficult to diagnose, as magnetic resonance imaging (MRI) of the brain is often unremarkable several weeks after its onset. This case of ODS occurred when normonatremia led to hypernatremia, as a result of rhabdomyolysis and hyperosmolar hyperglycemic syndrome. Diagnosis was made based on the MRI brain findings.

Development of monomorphic ventricular tachycardia in a patient with fever-induced Brugada syndrome.

A 50-year-old woman visited the emergency department with a high fever due to pneumonia. Incessant monomorphic ventricular tachycardia occurred and was terminated by intravenous lidocaine. Her ECG during sinus rhythm demonstrated ST segment elevation suggestive of Brugada syndrome (BS). An intensive examination could not detect any structural disease, and typical coved-type ST elevation was unmasked by a pilsicainide injection leading to a diagnosis of BS. An ICD was implanted for secondary prevention of ventricular arrhythmia. The patient has been free from any recurrences of arrhythmia for 3 years.

Mismatch between right- and left-sided filling pressures in heart failure patients with preserved ejection fraction.

BACKGROUND: Mismatch between right- and left-sided filling pressures is poorly understood in heart failure with preserved ejection fraction (HFpEF). METHODS AND RESULTS: We retrospectively analyzed 170 patients with HFpEF (EF≥40%) who underwent right heart catheterization. Low match (right atrial pressure [RAP] < 10 mm Hg and pulmonary capillary wedge pressure [PCWP] < 22 mm Hg) was 76%, high match (RAP ≥ 10 mm Hg and PCWP ≥ 22 mm Hg) was 6.5%, high-R mismatch (RAP ≥ 10 mm Hg and PCWP < 22 mm Hg) was 12%, and high-L mismatch (RAP < 10 mm Hg and PCWP ≥ 22 mm Hg) was 5.9%. Elevated PCWP was a significant predictor of the composite endpoint of death or HF hospitalization within 12months (hazard ratio 5.40, 95% confidence interval 2.17-12.5, p<0.001). Elevated RAP was not significantly associated with worse outcomes. Pulmonary artery systolic pressure (PASP) and diastolic pressure (PADP) showed strong correlations with PCWP (PASP, r=0.738, p<0.001; PADP, r=0.834, p<0.001; RAP, r=0.638, p<0.001, respectively). CONCLUSIONS: Discordance exists between right- and left-sided filling pressures in HFpEF. Physicians may utilize pulmonary artery pressure to evaluate left-sided filling pressure, which is a significant predictor of prognosis.